Degree Of Tissue Damage Research Articles

Double human bite

Bite wounds are common from dogs, cats and humans, subsequent infection depending on the degree of tissue damage and the delay in seeking treatment. Antibacterial therapy is either oral or parenteral depending on the degree of infection, with surgical wound debridement if necessary. Tetanus and anti-rabies treatment need also to be considered. The organisms from cats and dogs are P. multocida, Staph. aureus, Strep. spp., Prevotella spp. and Fusobacterium spp. Those from human bites are; Strep. spp., Staph. aureus, Prevotella spp, Peptostrep. spp. and Fusobacterium spp., especially Vincent s organisms; F. fusiforme and occasionally Borrelia vincenti.

Map‐ISODATA demarcates regional response to combination rt‐PA and 7E3 F(ab′)2 treatment of embolic stroke in the rat

To investigate the ability of map-ISODATA (Iterative Self-Organizing Data Analysis Technique) to classify the different categories of ischemic damage in the lesion and to evaluate a combined (thrombolysis plus antiplatelet) treatment efficacy in an embolic stroke of rat. Rats subjected to embolic stroke with (N=12) and without (N=10) rt-PA and 7E3 F(ab')2 treatment (4 hours after embolization) were followed (at 2, 24, and 48 hours post-MCAO) with magnetic resonance imaging (MRI) using T1, T2, and apparent diffusion coefficient of water (ADCw). ISODATA was computed from T1, T2, and ADCw maps. The signatures characterized by the map-ISODATA were compared with histological quantitative evaluation and were employed to demarcate the specific regions in the lesion. The signature described by map-ISODATA is highly correlated with the degree of tissue damage in the lesion and can distinguish the severity of ischemic tissue injury. Based upon map-ISODATA, ischemic lesion area can be divided into three specific regions, each characterized by a distinct evolution of injury and treatment response. The combined treatment significantly reduces the lesion size between 24 and 48 hours and improves the outcome 48 hours post-MCAO compared with the control group. Map-ISODATA provides an accurate means to identify lesion area, to distinguish ischemic damage, and to detect treatment response. 7E3 F(ab')2 extends the rt-PA treatment window to at least four hours after the onset of embolic stroke of rat.

Systemic stress responses in patients undergoing surgery for benign prostatic hyperplasia

To determine differences in systemic stress responses in patients undergoing three different types of surgery for benign prostatic hyperplasia (BPH), evaluated by measuring levels of stress variables, i.e. cortisol; acute-phase reactants, i.e. C-reactive protein (CRP) and fibrinogen; and antioxidants, i.e. total antioxidant status (TAS) and superoxide dismutase (SOD). The study included 80 patients who fulfilled the inclusion criteria for surgery for BPH. Based on an ultrasonographic estimate of the prostate volume before surgery, all patients were allocated to one of three groups; group 1, prostate < or = 30 g and treated with transurethral incision of the prostate (TUIP); group 2, prostate 30-80 g, treated with transurethral resection of the prostate (TURP); and group 3, prostate >80 g, treated with a suprapubic transvesical prostatectomy (TP). Blood samples were taken from each patient on the day before and the day after surgery, and the acute-phase reactants and antioxidants measured; cortisol concentrations were also measured in 24-h urine samples the day before and 3 days after surgery. There were significantly higher levels of cortisol, CRP and TAS, and significantly lower levels of fibrinogen and SOD in all study groups after surgery than before. Surgery and associated conditions, e.g. excitement, fear, blood loss, etc., lead to traumatic and oxidative stress, followed by a strong systemic stress response during and after surgery. Low fibrinogen levels after surgery had a different pattern from the other acute-phase reactants, as a result of increased fibrinolytic activity after TURP and TP. The extent of the systemic stress response correlated fairly well with the degree of tissue damage, which differed in the three groups. Suprapubic TP caused the most tissue trauma and triggered the strongest systemic stress response. This response was moderate after TURP, while TUIP (a minor intervention) caused the least stress. Specific changes in stress markers could be used to improve surgery for BPH. Whether there is a benefit of antioxidant therapy during surgery for BPH should be evaluated in further studies.

Neuroregulatory events follow adaptive immune-mediated elimination of HIV-1-infected macrophages: studies in a murine model of viral encephalitis.

HIV-1-specific cellular immunity serves to eliminate infected cells and disease. However, how this process specifically affects the CNS is poorly understood. To mirror the regulatory events that occur in human brain after HIV-1 infection, a murine model of viral encephalitis was used to study relationships, over time, among lymphocyte-mediated infected cell elimination, innate immune responses, and neuropathology. Nonobese diabetic SCID mice were reconstituted with human PBL and a focal encephalitis induced by intracranial injection of autologous HIV-1-infected, monocyte-derived macrophages (MDM). On days 7, 14, and 21 after MDM injection into the basal ganglia, the numbers of human lymphocytes and mouse monocytes, virus-infected MDM, glial (astrocyte and microglial) responses, cytokines, inducible NO (iNOS), neurotrophic factors, and neuronal Ags were determined in brain by immunohistochemistry, real-time PCR, and Western blot assays. Microglia activation, astrocytosis, proinflammatory cytokines, and iNOS expression accompanied the loss of neuronal Ags. This followed entry of human lymphocytes and mouse monocytes into the brain on days 7 and 14. Elimination of virus-infected human MDM, expression of IL-10, neurotropins, and a down-regulation of iNOS coincided with brain tissue restoration. Our results demonstrate that the degree of tissue damage and repair parallels the presence of infected macrophages and effectors of innate and adaptive immunity. This murine model of HIV-1 encephalitis can be useful in elucidating the role played by innate and adaptive immunity in disease progression and resolution.

Pressure ulcer grading tools: how reliable are they?

Use of grading tools has become routine, yet their reliability and validity have not been rigorously researched and they should not be used to monitor healing. Also, many require a level of expertise that is beyond the capability of general nurses.

Evaluation of adrenomedullin levels in renal parenchyma subjected to extracorporeal shockwave lithotripsy.

Despite its safety and efficacy, the traumatic effects of high-energy shock waves (HESW) on renal morphology and function during long-term follow-up have yet to be elucidated. Although the main target of shock waves is the stone located in the kidney, the surrounding tissue and other organs are also subjected to trauma during this procedure. In contrast to renal blood flow evaluation after shock wave treatment, ischemic development, causing varying degrees of damage at the tissue level, has not been well evaluated. The renoprotective peptide adrenomedullin (AM) is a potent vasorelaxing, natriuretic and cell growth modulating peptide, which is thought to act as an autocrine/paracrine regulator in renal glomeruli and tubules. In this experimental study, renal parenchymal AM levels were assessed in an attempt to evaluate the effect of HESW on the tissue levels of this peptide, which may be responsible for the regulation of ischemia induced by extracorporeal shock wave lithotripsy(ESWL), in a rabbit model. Thirty white New Zealand rabbits, each weighing 3-5 kg were used. The animals were divided into three main groups, and varying numbers of shock waves (1000, 1500, 2000) were applied under fluoroscopic localization to the same kidney of all animals. Ketamine HCl anesthesia was administered (15-20 mg/kg) and all of the procedures were performed with a Multimed 2000 lithotriptor. Untreated contralateral kidneys were evaluated as controls. Following HESW application, the treated and untreated kidneys of each animal were removed through bilateral flank incisions under ketamine HCl anesthesia after 24 h and 7 days, respectively. Tissue AM levels were assessed with immunohistochemistry. During the early follow-up period (24 h), both treated and untreated kidneys showed a moderate to high degree of AM positivity. The number of tubules stained with AM increased as the number of shock waves increased and the expression of this protein became evident, possibly due to a higher degree of tissue damage. Additionally, a limited degree of AM positivity was noted in the contralateral kidneys although this was not as evident as the positivity seen in the treated kidneys. Assessment of tissue AM levels during late follow-up (7 days) in both kidneys demonstrated a moderate or limited degree of positivity in the treated kidneys. Limited or no positivity could be demonstrated in the contralateral kidneys at this time. Taking the certain traumatic effects of HESW, which causes transient ischemia during ESWL, into account, we conclude that the application of HESW results in a transient decrease in renal perfusion, causing ischemic injury in treated as well as in contralateral (untreated) kidneys. This ischemic event lasts for a short time and seemed to be dose- and time-dependent. Increased tissue levels of AM appear to be a potential defence against ESWL induced ischemia.

Aquaporin‐4 water channel expression in human vasogenic brain oedema

A number of brain lesions result in brain oedema formation. This oedema is considered to be vasogenic in nature, resulting from breakdown of the blood–brain barrier. Brain microvessels are surrounded by astrocyte foot processes that express the water channel protein aquaporin 4 (aqp4). Aqp4 has been implicated in the formation of vasogenic oedema in animal models, but little is known about its involvement in vasogenic oedema in man. Therefore formalin‐fixed samples of a variety of brain lesions that give rise to brain oedema were obtained from 17 patients who underwent craniotomy at atkinson morley’s hospital during 1993–9. Immunocytochemistry was then performed on the samples using a polyclonal aqp4 antibody (ab3068, chemicon) visualised with immunoperoxidase and diaminobenzidine hydrochloride. In histologically normal cerebral cortex (n = 1) aqp4 immunoreactivity was restricted to astrocyte foot processes lining the pial membrane and surrounding some microvessels. In contused cortex (n = 3) astrocyte aqp4 expression was up‐regulated in accordance with the degree of tissue damage and the severity of oedema, assessed by contrast enhancement on ct. Aqp4 immunoreactivity was not present in nonastrocytic tumour cells including adenocarcinoma (n = 4), meningioma (n = 4), oligodendroglioma (n = 1) and medulloblastoma (n = 1). However diffuse aqp4 immunoreactivity was present in cells with the morphology of reactive astrocytes at the periphery of these tumours and occasionally ‘trapped’ within them. In addition up‐regulation of aqp4 immunoreactivity was observed in astrocyte end feet surrounding the microvessels in the perimeningioma cortex. Diffuse aqp4 immunoreactivity was observed in a subependyal astrocytoma (n = 1). Strong aqp4 immunolabelling of astrocytes was observed in cerebral cortex affected by bacterial meningitis (n = 1). Up‐regulation of aqp4 immunoreactivity was also observed in the foot processes of astrocytes lining the pial membrane and surrounding microvessels in this tissue. Up‐regulation of aqp4 immunoreactivity was not observed in brain tissue affected by subarachnoid haemorrhage (n = 1), from a patient who did not show any evidence of oedema on ct. Therefore brain lesions with different aetiologies that result in vasogenic brain oedema appear to cause a similar up‐regulation of aqp4 expression in astrocytes associated with the lesions. These results suggest that aqp4 up‐regulation in astrocytes may be part of a ‘final common pathway’ leading to oedema formation.

Gene transfer into retinal ganglion cells by in vivo electroporation: a new approach

We developed a new in vivo electroporation method to deliver genes into retinal ganglion cells (RGCs). Efficiency and degree of tissue damage were evaluated using green fluorescent protein (GFP) gene and TUNEL. Soon after the intravitreous injection of the GFP gene, electroporation (five electric pulses of 99 ms duration each and 12 V/cm delivered twice 5 min apart) was carried out on the adult rat eyeball with the aid of tweezer-type disc electrodes attached to corneal (cathode) and scleral (anode) surfaces. GFP expression, exhibiting a maximum on day 7, was detectable for up to 21 days. DiI retrograde labeling of RGCs showed that 41.5% of the total ganglion cells in the electroinjected area were GFP-positive. Therefore, this new method may be a useful tool for the delivery of genes into RGCs.

The common ovine Shiga toxin 2-containing Escherichia coli serotypes and human isolates of the same serotypes possess a Stx2d toxin type.

Shiga toxin 2 (Stx2) has been reported as the main Shiga toxin associated with human disease. In addition, the Stx2 toxin type can have a profound impact on the degree of tissue damage in animal models. We have characterized the stx(2) subtype of 168 Shiga toxin-producing Escherichia coli (STEC) isolates of which 146 were derived from ovine sources (principally feces and meat) and 22 were isolated from humans. The ovine STEC isolates were of serotypes that have been shown to occur commonly in the gastrointestinal tract of healthy sheep. The major stx(2) subtype in the ovine isolates was shown to be stx(2d-Ount) (119 of 146 [81.5%]) and was predominantly associated with serotypes O75:H(-)/H8/H40, O91:H(-), O123:H(-), O128:H2, and OR:H2. However, 17 of 18 (94.4%) ovine isolates of serotype O5:H(-) possessed a stx(2d-O111/OX3a) subtype. Furthermore, STEC isolates of serotypes commonly found in sheep and recovered from both clinical and nonclinical human infections also contained a stx(2d) (stx(2d-Ount/O111/OX3a)) subtype. These studies suggest that a specific stx(2) subtype(s) associates with serotype and may have important epidemiological implications for tracing sources of E. coli during outbreaks of STEC-associated diseases in humans.

Riluzole reduces brain swelling and contusion volume in rats following controlled cortical impact injury.

Modulation of the glutamatergic and excitotoxic pathway may attenuate secondary damage following traumatic brain injury by reducing presynaptic glutamate release and blocking sodium channels in their inactivated state. The aim of the present study was to investigate the neuroprotective potential of riluzole in traumatic brain-injured rats. A left temporoparietal contusion was induced in 70 male Sprague-Dawley rats (controlled cortical impact injury). Riluzole (8 mg/kg body weight) was given 30 min, and 6, 24, and 30 h after trauma, while control rats received physiological saline. Experiments were performed at two different degrees of trauma severity as defined by penetration depth of the impactor rod (1 vs. 1.5 mm) with the aim of investigating impact of severity of tissue damage on the neuroprotective potential of riluzole. At 48 h after trauma, brains were removed to determine hemispheric swelling and water content and to assess cortical contusion volume. Before brain removal cisternal cerebrospinal fluid (CSF) was collected in all rats to determine the effects of riluzole on substances associated with edema formation. For this, the excitatory transmitter glutamate, the volume-regulatory amino acid taurine, and the ATP-degradation product hypoxanthine were analyzed by high-performance liquid chromatography. Overall, the degree of tissue damage seems to influence the neuroprotective potential of riluzole. In rats with a less severe trauma (1-mm penetration depth), hemispheric swelling, cerebral water content of the traumatized hemisphere and cortical contusion volume were significantly reduced under riluzole compared to controls (p < 0.05). In rats with a more severe trauma (1.5-mm penetration depth), the neuroprotective effect of riluzole failed to reach statistical significance. Following trauma, CSF glutamate, taurine, and hypoxanthine levels were significantly increased compared to nontraumatized rats (p < 0.001). However, these neurochemical parameters as measured in cisternal CSF failed to reflect trauma-dependent increases in severity of tissue damage and did not reveal riluzole-mediated neuroprotection. Under the present study design, riluzole significantly reduced brain edema formation and contusion volume in rats subjected to a mild focal cortical contusion.

Moderate hypothermia prevents cell injury in rats with severe haemorrhagic shock

Abstract Background This study aimed to evaluate a possible protective and therapeutic effect of mild to moderate hypothermia in severe haemorrhagic shock. Brainstem is one of the most sensitive tissues to oxidative stress in the early phase of haemorrhagic shock. The haemorrhagic oxidative stress at various core temperatures was studied using reduced glutathione (GSH) levels and thiobarbituric acid reactive substances (TBARS) as markers of lipid peroxidation in brainstem homogenate. Methods Forty rats were divided into four groups, of which one constituted the non-bleeding normothermia control group. In all of the three study groups, the rats were bled to 40 per cent of their estimated blood volume while they were being held at normothermia, mild (32°C) or moderate (28°C) hypothermia. Mean arterial pressure, rectal temperature, heart and breathing rates were recorded during the procedures. After 1 h of shock, tissue samples were removed by craniectomy. Results The tissue levels of TBARS increased significantly in normothermic and mildly hypothermic haemorrhagic shock groups (10·74 and 8·26 nmol g−1) compared with control (3·50 nmol g−1) (P &amp;lt; 0·001). However, the tissue TBARS level in the moderately hypothermic group was only minimally increased (4·53 nmol g−1). GSH levels fell slightly in normothermic and mildly hypothermic bleeding rats, and were unchanged in moderately hypothermic rats. Conclusion The TBARS level, which was a predictor of oxidant damage, changed slightly during severe haemorrhagic shock when the rats were moderately hypothermic. Hypothermia had a protective effect against cell injury during haemorrhagic shock. Tissue TBARS levels correlated well with the degree of tissue damage; lower levels suggested hypothermic protection.

The Myriad Plant Responses to Herbivores.

Plant responses to herbivores are complex. Genes activated on herbivore attack are strongly correlated with the mode of herbivore feeding and the degree of tissue damage at the feeding site. Phloem-feeding whiteflies and aphids that produce little injury to plant foliage are perceived as pathogens and activate the salicylic acid (SA)-dependent and jasmonic acid (JA)/ethylene-dependent signaling pathways. Differential expression of plant genes in response to closely related insect species suggest that some elicitors generated by phloem-feeding insects are species-specific and are dependent on the herbivore's developmental stage. Other elicitors for defense-gene activation are likely to be more ubiquitous. Analogies to the pathogen-incompatible reactions are found. Chewing insects such as caterpillars and beetles and cell-content feeders such as mites and thrips cause more extensive tissue damage and activate wound-signaling pathways. Herbivore feeding is not equivalent to mechanical wounding. Wound responses are a part of the induced responses that accompany herbivore feeding. Herbivores induce direct defenses that interfere with herbivore feeding, growth and development, fecundity, and fertility. In addition, herbivores induce an array of volatiles that creates an indirect mechanism of defense. Volatile blends provide specific cues to attract herbivore parasites and predators to infested plants. The nature of the elicitors for volatile production is discussed.

Effect of trephination technique on the ultrastructure of corneal transplants: guided trephine system vposterior punch technique

AIMDifferent trephination methods may lead to differences in degree of tissue damage and endothelial cell loss, which both influence the outcome of penetrating keratoplasty. Light, transmission, and scanning electron microscopy...

Specific mucosal immunity in the pathophysiology of bacterial prostatitis in a rat model

Mucosal immunity was established in the rat prostate by stimulating the common mucosal system through serosal exposure of formalin-killed Escherichia coli. Immunized but not sham-immunized rats developed bacterial specific IgG and IgA in prostatic fluid, and IgA in urine. Immunized (n = 21) and sham-immunized control rats (n = 30) were challenged by transurethral injection of E. coli into the prostate ducts. Mortality, gross and microscopic pathology, tissue bacterial counts, bacterial associated immunoglobulins, and antibody titers in serum and urine were assessed at 7 days following the challenge. Increased E. coli specific immunoglobulin titers were seen in immunized rats, and E. coli, but not Proteus, found in the prostates of immunized animals were coated with IgG and IgA. Immunization protected against toxaemia and septicemia, seen as a rare complication of acute prostatitis, but did not protect against acute prostatitis, nor alter the degree of tissue damage seen in the rat model.

Dissolution of nickel and tissue response observed by X-ray scanning analytical microscopy

The recently developed X-ray scanning analytical microscope (XSAM) was applied for the analysis of the soft tissue of rat in which Ni was implanted and serious inflammation occurred. Our aim is to investigate the relationship between tissue response and elemental distributions. The XSAM observation was conducted in air without pretreatment and staining of samples. Mapping images of P, S, Ca, Fe and Ni, which were the elements with low concentration in soft tissue, were obtained from the soft tissue blocks of rat where Ni was implanted. S mapping image showed the localization of S in muscle and in hairs. Ca mapping image showed the localization of Ca in muscle and hair roots. Fe distribution was also observed and the localized area was consistent with the hemorrhagic area. The Ni dissolution area was clearly detected around the Ni implant. Comparison with the histological observation showed that the Ni dispersed area was consistent with the inflammatory area and the degree of tissue damage was closely related to the dissolved Ni concentration.

Gamma radiation and MC540 photosensitization of melanoma in the hamster's eye.

The purpose of this study was to evaluate the effects of cobalt-60 gamma-radiation and argon laser irradiation using injected merocyanine (MC540) as a photosensitizer on pigmented and non-pigmented Bomirski hamster melanomas growing in the eye. The animals were treated with one of four regimens, receiving gamma-irradiation only, photosensitization only, a combination of gamma-irradiation and photosensitization, or a combined time-fractionated treatment. Tumours were exposed to laser light 24 h after injection, when the photosensitizing dye concentration was highest. The degree of tissue damage was evaluated by observation of the area for necrosis, interruption of blood circulation, and the shape and dissemination of the tumour cells. Additionally, tumour growth was monitored through the measurement of tumour volume and also calculated from histological cross sections on the assumption that the tumour morphology is hemi-ellipsoidal. A single treatment of tumours by a combination of photodynamic therapy and ionizing radiation resulted in an additive effect, inhibiting tumour growth for 2-4 days. A time-fractionated treatment, given four times every 24 h, markedly delayed tumour growth for up to 6 weeks. The results indicate that MC540-mediated photodynamic treatment in combination with gamma-radiation exerts a significant therapeutic effect on a rapidly growing melanoma.

Donor-specific cytotoxic lymphocyte activity from bronchoalveolar lavage during acute canine lung allograft rejection.

We investigated the relationship between acute lung rejection and donor-specific cytotoxic activity (DSCA) in recipient's lymphocytes obtained from bronchoalveolar lavage (BAL). A total of 26 mongrel dogs underwent left lung allotransplantation. Dogs received either no immunosuppressive treatment (group I), cyclosporine (group II), or cyclosporine and methylprednisolone for evidence of acute rejection (group III). DSCA was measured by a 51Cr release assay, using lymphocytes from BAL samples as effector cells and 51Cr-labeled donor skin fibroblasts as target cells. The pathologic findings of the transplanted lungs were classified according to the working formulation for classification and grading of pulmonary rejection. In addition, the degree of cellular infiltration in the perivascular, peribronchial, interstitial, and intraalveolar areas was determined based on an infiltration score. DSCA in BAL samples was elevated during mild, moderate and severe acute rejection. The accuracy of the diagnosis of mild or moderate rejection was 92.3% at effector:target (E:T) ratios of 100:1 and 50:1. The DSCA in the BAL fluid and the total infiltration score were correlated closely with correlation coefficients of 0.859 and 0.828 at E:T ratios of 100:1 in group I and group II dogs, respectively. Lung aeration improved and DSCA decreased with methylprednisolone therapy in three of four dogs with grade 2 rejection. There is a direct relationship between the DSCA in BAL fluid and the degree of tissue damage caused by acute rejection. The DSCA can be detected by a 51Cr release assay which may hold promise for future clinical applications.

Activation of mRNA expression of collagen, collagenase and its inhibitor on renal biopsy specimens in patients with IgA nephropathy

Summary: In situ hybridization of mRNA for collagen IV, collagen VI, stromelysin (MMP‐3) and TIMP1 was examined in renal biopsy specimens from patients with IgA nephropathy (IgAN) or diabetic nephropathy with various degrees of tissue damage. The majority of cells in the glomeruli expressed these mRNA almost simultaneously, but a few cells demonstrated positive expression for only one of these probes. There was a parallel relationship between the degree of tissue damage and that of mRNA expressions of these probes in patients with IgAN, while patients with diabetic nephropathy showed a reverse relationship between these two parameters. It is concluded that patients with mesangial proliferative glomerulonephritis expressed mRNA for collagen collagenase and its inhibitor in the glomeruli in parallel with the progress of tissue damage. In contrast, glomerular samples from patients with diabetic nephropathy showed that there was an inverse relationship between tissue damage and expression of mRNA. It is concluded that expression of collagen, collagenase and its inhibitor parallels the progression of glomerular changes in IgAN, but such parallel expression was not observed in patients with diabetic nephropathy.

Molecular approaches to the study of renal disease

Summary: Recent developments in cell biology and molecular biology have provided new techniques for molecular studies on renal diseases. the in situ hybridization technique demonstrates the site and the degree of gene expression of various cytokines and regulating proteins associated with the altered function of the glomeruli. It is not known, however, if the expression of these genes is different among various glomerular diseases. the aim of this study was to elucidate the disease specific phenomena in glomerular gene expression. Renal biopsy specimens were obtained from patients with diabetic nephropathy, and IgA nephropathy. the degree of tissue damage as well as the levels of various clinical parameters were matched between these two groups. In situ hybridization of mRNA in renal tissues for transforming growth factor (TGF)‐β, storomelysin (MMP‐3) and tissue inhibitor of metalloproteinase (TIMP‐1) were performed using nonradioactive digoxigenin (DIG)‐labelled oligonucleotide probes. In parallel studies, renal biopsy specimens were stained with monoclonal antibody against advanced glycated end‐products (AGE). the results demonstrated that the distribution of mRNA expression of TGF‐β was similar between these two diseases, but the expression of MMP‐3 and TIMP‐1 was parallel with the degree of tissue damage in patients with IgA nephropathy while it was diminished in patients with an advanced degree of tissue damage due to diabetic nephropathy. Positive staining of renal tissues with anti‐AGE antibody was only observed in patients with diabetic nephropathy. It is concluded that glycation of renal structural proteins might interfere with their metabolism by enzymes and their inhibitors, while a cytokine responsible for mesangial expansion was similarly expressed.

Cellular immunity in IgA nephropathy

Summary: A comprehensive study on the role of various cytokines in the regulation of IgA synthesis and progression of glomerular damage in IgA nephropathy was attempted. Semi‐quantitative PCR for IL‐I, IL‐2, IL‐4, IL‐6, IL‐10, IL‐12, interferon (IFN)‐γ, transforming growth factor (TGF)‐β, tumour necrosis factor (TNF)‐α, platelet derived growth factor (PDGF) and monocyte chemoattractant protein‐1 (MCP‐1) was performed. In parallel studies, protein production of some cytokines was also determined. It was demonstrated that IL‐4, IFN‐γ and presumably IL‐12 expressed predominantly in peripheral blood mononuclear cells in patients with IgA nephropathy. Some positive correlations between the mRNA expression of these cytokines and the degree of tissue damage were observed. It was concluded that these cytokines may play some role in the alteration of cellular immunity in this disease.